Coxsackievirus B-3 myocarditis. Acute and chronic forms of the disease caused by different immunopathogenic mechanisms.

摘要: Male BALB/c, DBA/2 and A mice inoculated with a myocarditic variant of coxsackievirus group B, Type 3 (CVB3) developed three distinct patterns myocarditis. Most BALB/c all acute cardiac inflammation lasting only 2 weeks, while animals consistently showed twice as much myocardial damage the other two strains, active myocarditis continuing for 56 days after virus inoculation. Although elimination from heart was also delayed in mice, immunopathogenic, not viral, mechanisms caused injury strains. In vivo depletion L3T4+ (T helper) Lyt 2+ cytolytic/suppressor) cells using monoclonal antibodies that depended predominantly on cells, both cells. IgM reactive (HRAs) occurred IgG HRAs were detected mice. Presumably, antibody pathogenic this system. These data suggest host's genetic makeup determines type immune response to CVB3 infection therefore pattern which develops.